ArticleNucleic acids research2000
Activation of c-myc promoter P1 by immunoglobulin kappa gene enhancers in Burkitt lymphoma: functional characterization of the intron enhancer motifs kappaB, E box 1 and E box 2, and of the 3' enhancer motif PU.
Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Review
- JNK/AP1 Pathway Regulates MYC Expression and BCR Signaling through Ig Enhancers in Burkitt Lymphoma Cells.Journal of Cancer · 2020Article
- Transcriptional Dynamics at Brain Enhancers: from Functional Specialization to Neurodegeneration.Current neurology and neuroscience reports · 2016Review
- LMP1-augmented kappa intron enhancer activity contributes to upregulation expression of Ig kappa light chain via NF-kappaB and AP-1 pathways in nasopharyngeal carcinoma cells.Molecular cancer · 2009Article
- Comparative characterization of a temperature responsive gene (lactate dehydrogenase-B, ldh-b) in two congeneric tropical fish, Lates calcarifer and Lates niloticus.International journal of biological sciences · 2009Article
- Activation of the c-myc p1 promoter in Burkitt's lymphoma by the hs3 immunoglobulin heavy-chain gene enhancer.Leukemia · 2007Article
- Mapping of MYC breakpoints in 8q24 rearrangements involving non-immunoglobulin partners in B-cell lymphomas.Leukemia · 2007Article
- Article
- Translocations involving c-myc and c-myc function.Oncogene · 2001Review
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Deregulated expression of the proto-oncogene c- myc in Burkitt lymphoma (BL) cells carrying a t(2;8) translocation is mediated by a synergistic interaction of the translocated immunoglobulin (Ig) kappa gene intron (kappaEi) and 3' (kappaE3') enhancers and characterized by a strong activation of the promoter P1. We have investigated the functional role of distinct kappa enhancer sequence motifs in P1 activation on both mini-chromosomes and reporter gene constructs. Stable and transient transfections of BL cells revealed critical roles of the kappaEi and kappaE3' elements kappaB and PU, respectively. Joint mutation of kappaB and PU completely abolished P1 activity, implying that an interaction of kappaB- and PU-binding factors is essential for the enhancer synergism. Mutation of the E box 1 and E box 2 motifs markedly decreased P1 activity in transient but not in stable transfection experiments. Co-expression of the NF-kappaB subunit p65(RelA) and Sp1, an essential factor for P1 transcription, in Drosophila melanogaster SL2 cells synergistically enhanced promoter activity. Our results support a model which proposes cross-talk between promoter and enhancer binding factors as the basic mechanism for kappa enhancer-mediated c- myc activation in BL cells.
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